Studies of consomic mice bearing the Y chromosome of the BXSB mouse.

Studies of consomic mice bearing the Y chromosome of the BXSB mouse.
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对携带 BXSB 小鼠 Y 染色体的体鼠的研究。

DOI:
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发表时间:
1985
影响因子:
4.4
通讯作者:
A. Steinberg
A. Steinberg
中科院分区:
医学2区
文献类型:
--
作者:
C. C. Hudgins;R. T. Steinberg;D. Klinman;M. J. Reeves;A. Steinberg

文献摘要

被引文献

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先前的研究表明,BXSB小鼠的Y染色体可导致近交系BXSB小鼠和F1杂交种的自身免疫加速。为了进一步研究BXSB-Y的作用,我们研究了三组y -经济小鼠,NZB。BXSB-Y NZW。BXSB-Y和CBA/J。BXSB-Y分别由来自非BXSB亲本的背景基因和来自BXSB小鼠的Y染色体组成。评估BXSB-Y对自身抗体产生、免疫病理和生存的影响。我们发现CBA/J。BXSB-Y小鼠与对照CBA/J雄性小鼠差异不大。相比之下,纽元。BXSB- y雄性小鼠的肾脏和心脏疾病和早期死亡加速,类似于先前报道的(NZW X BXSB)F1小鼠。NZB。BXSB-Y男性抗红细胞自身抗体加速,但抗dna不加速。它们的寿命几乎和NZB小鼠一样长。BXSB- y在所有经济小鼠中都存在,通过与BXSB雌性经济小鼠杂交证实,并且在雄性后代中显示加速疾病。本研究表明,BXSB-Y染色体自身免疫加速因子不是单独起作用,而是通过其他基因起作用,并且对不同遗传背景的影响是不同的。这些研究对人类狼疮有启示;它们也为BXSB-Y及其作用基因的未来分子生物学研究提供了基础。
Previous studies have demonstrated that the Y chromosome of the BXSB mouse can lead to accelerated autoimmunity in inbred BXSB mice and in F1 hybrids. To additionally study the effects of the BXSB-Y, we have studied three sets of Y-consomic mice, NZB.BXSB-Y, NZW.BXSB-Y, and CBA/J.BXSB-Y, each consisting of background genes from the non-BXSB parent and the Y chromosome from the BXSB mouse. The effect of the BXSB-Y on autoantibody production, immunopathology, and survival was assessed. We found that the CBA/J.BXSB-Y mice showed few differences from control CBA/J males. In contrast, NZW.BXSB-Y males had accelerated renal and cardiac disease and early death, resembling that previously reported for (NZW X BXSB)F1 mice. NZB.BXSB-Y males had accelerated anti-erythrocyte autoantibodies but not accelerated anti-DNA. They lived almost as long as NZB mice. The presence of the BXSB-Y in all of the consomic mice was confirmed by crossing the consomic mice with BXSB females and demonstrating accelerated disease in the male offspring. This study demonstrates that the BXSB-Y chromosome autoimmune accelerating factor does not act alone but operates through other genes, and that the effects on different genetic backgrounds are different. The studies have implications for human lupus; they also provide a basis for future molecular biology studies of the BXSB-Y and the genes upon which it acts.